Abstract

Cerebral palsy (CP), defined as a group of nonprogressive disorders of movement and posture, is the most
common cause of severe neurodisability in children. Understanding its physiopathology is crucial to developing
some protective strategies. Interruption of oxygen supply to the fetus or brain asphyxia was classically
considered to be the main causal factor explaining later CP. However several ante-, peri-, and postnatal factors
could be involved in the origins of CP syndromes. Congenital malformations are rarely identified. CP is most
often the result of environmental factors, which might interact with genetic vulnerabilities, and could be severe
enough to cause the destructive injuries visible with standard imaging (i.e., ultrasonographic study or MRI),
predominantly in the white matter in preterm infants and in the gray matter and the brainstem nuclei in full-term
newborns. Moreover they act on an immature brain and could alter the remarkable series of developmental
events. Biochemical key factors originating in cell death or cell process loss, observed in hypoxic-ischemic as
well as inflammatory conditions, are excessive production of proinflammatory cytokines, oxidative stress,
maternal growth factor deprivation, extracellular matrix modifications, and excessive release of glutamate,
triggering the excitotoxic cascade. Only two strategies have succeeded in decreasing CP in 2-year-old children:
hypothermia in full-term newborns with moderate neonatal encephalopathy and administration of magnesium
sulfate to mothers in preterm labor.
Copyright 2013 Elsevier B.V. All rights reserved.
Pathophysiology
Varies depending on the aetiology, which includes overt structural lesions of the brain or less visible lesions that
result from antenatal, neonatal, and postnatal events. Other factors such as toxins, infections, multiple births,
and maternal health also exert an influence. [12] Postnatal brain MRIs show abnormalities in up to 80% of
established cases of CP. [20] [21]
Severe compromise in oxygen and/or cerebral perfusion following birth trauma leads to hypoxic-ischaemic
encephalopathy. A similar neonatal encephalopathy can also occur with inflammatory conditions such as
maternal fever and infection. [22] [23] Between 26 and 34 weeks of gestation, selective vulnerability of the
periventricular white matter (e.g., to periventricular leukomalacia [PVL] or periventricular haemorrhage) occurs
involving the internal capsule. Fetal insults at this time may result in spastic diplegia. These white matter
changes are also found in 71.3% of children with spastic diplegia, 34.1% with spastic hemiplegia, and 35.1% of
those with spastic quadriplegia, despite 25% of these cases being term births. [20]
The corticospinal tract (shown in red), responsible
for voluntary motor controlPublic domain image
In spastic CP, impulses from the motor cortex (precentral gyrus) are compromised along their path via the
internal capsule to the spinal motor neurons and eventually to the site of action, the skeletal muscles. The
corticospinal (pyramidal) tracts initiate and carry impulses necessary for voluntary movement. Damage to the
primary motor cortex or the corticospinal tract impairs voluntary movement and fine motor control. Spasticity
appears to be a result of damage or abnormal input to the vestibular and reticular nuclei or their tracts, which
results in loss of inhibitory influences to the spinal motor neuron pools. Damage to the reticulospinal system
increases tone; damage to the vestibulospinal tract, which modulates anti-gravity skeletal activity and balance
reflexes, results in an increased extensor tone.
Lesions of the basal ganglia, commonly associated with parkinsonian-like syndromes, do not result in spasticity
but are involved in the dyskinetic forms of CP. Unique metabolic demands of the basal ganglia in the fetus at 38
to 40 weeks can result in dystonia or other movement disorders in the event of damage during this period. [24]
Severe hyperbilirubinaemia, now largely preventable, leads to damage to basal ganglia due to deposition of
bilirubin byproducts, causing dyskinesia. Ataxia and hypotonia are associated with damage to the cerebellum or
cerebellar pathways. [
The pathophysiology of cerebral palsy begins before birth. The cause of cerebral palsy is typically a brain injury
or abnormality that happens prenatally or during infancy. This disease causes problems with brain control of
muscles, leading to difficulties with posture, muscle tone, and movement.
A child born prematurely or with a low birth weight is at a higher risk for cerebral palsy. Maternal illness is
another risk factor, as are injuries or illnesses in the child's infancy.
Symptoms can vary greatly, but the condition is usually evident from a young age. Often, developmental delays
in motor abilities are the first sign. A person affected by cerebral palsy may show problems with muscle tone,
resulting in muscles that are too tight or too floppy. There may also be a lack of coordination, which can cause
difficulty walking or a struggle with fine motor movements. Some children have difficulty with eating, sucking,
and swallowing.
Brain damage, which is part of the pathophysiology of cerebral palsy, is not restricted to muscle control, and so
people with this disorder will show deficits in other areas, such as language. There may also be problems with
the senses, especially vision and hearing. Some people may suffer from mental retardation or seizures.
Maternal illnesses, especially infections, can lead to this condition, as can genetic mutations that affect the
brain. A prenatal stroke that prevents blood flow to part of the brain can also cause cerebral palsy. Head injury
in an infant, from a car accident, abuse, or a different trauma, is another possible cause.
Since the muscles can be too tense for long periods of time, the normally stretchy tissue can be replaced by
tissue that doesn't stretch, called a contracture. This also causes the muscles to get shorter. Constant pressure on
the joints from muscle tightness can cause osteoarthritis, which can be very painful. If a person with cerebral
palsy has difficulty eating or swallowing, he or she may suffer from malnutrition. Cerebral palsy can severely
interfere with a persons ability to function normally, and so can lead to depression.
There is no known cure for cerebral palsy. If a person suffers from muscle spasms, certain medications can be
used to keep them under control. Physical therapy to exercise and stretch the muscles can help a person walk
normally and prevent contractures. If there are severe contractures or joint abnormalities, surgery may be
necessary.
Cerebral Palsy
Jyotsna
Gandhi
Department of Obstetrics and Gynecology, Elmhurst Hospital Center. Mount Sinal School of Medicine.
One Guystave L. Levy Place. Box 1116, New York. (NY) USA.
J Obstet Gynecol India Vol. 57, No. 1 : January/February 2007 Pg 27-36
REVIEW
AR
TICLE
The Journal of
Obstetrics and Gynecology
of India
Paper received on 01/10/2006 ; accepted on 06/11/2006
Correspondence :
Dr. Jyotsna Gandhi
472-5173
1 Candlewood Court
Scarsdale, NY 10583. USA.
Tel. (718) 344-5366, Fax (718) 344-2117.
Incidence
Cerebral palsy
(CP)
is the most common congenital
neurologic disorder. The world wide prevalence of cerebral
palsy is 2-2.5/1000 live births
1
. In the past it was thought to
occur as a result of acute intrapartum hypoxic events. Recent
epidemiological studies suggest that in only 10% of cases
this is true, and 90% of cases are due to chronic events or
congenital factors
2-4
.
Definition and criteria
CP is a chronic disability of central nervous system origin
characterized by aberrant movement and posture, appearing
early in life and associated with defect or lesion of the
immature brain.
Neonatal encephalopathy and hypoxic-ischemic
encephalopathy (HIE) have been defined in term and near
term infants as a group of criteria to collectively include
altered consciousness, tone, reflexes, feeding ability
respiration, and/or seizures, and may or may not result in
permanent neurologic injuries. Previous epidemiologic studies
show that only 19% of neonatal encephalopathy met old
nonstringent criteria for neonatal intrapartum hypoxia. CP
due to HIE must be preceded by neonatal encephalopathy.
Incidence of CP due to intrapartum asphyxia is only 1.6/
10,000 and 70% of neonatal encephalopathy occurs as a
result of prenatal events. Additionally intense intrapartum
monitoring in recent past has not reduced the incidence of
CP. However, in the past, birth asphyxia due to poor obstetric
management has been needlessly and without scientific basis
implicated medicolegaly.
Spastic quadriplegia, is the only type of CP associated with
intrapartum acute hypoxic events. Dyskinetic or ataxic CP
associated with learning problems, epilepsy, hyperactivity
disorders, attention deficit or mental retardation do not have
their origin in acute birth hypoxia.
History
Our current knowledge of cerebral palsy is highly enhanced
by both internationally published scientific evidence and a
joint project by the American College of Obstetricans and
Gynecologists and the American Academy of Pediatrics
(ACOG/AAP). A multidisciplinary International Cerebral Palsy
Task force of scientists and clinicians published a consensus
statement in 1999, which set out the criteria defining an
acute intrapartum hypoxic event necessary to have had
occurred prior to the onset of CP
5
. ACOG/AAP revised the
international template and updated the literature on the
pathogenesis and pathophysiology of neonatal
encephalopathy and cerebral palsy in 2003
6
(Table 1). Of
the nine criteria four when present together help to prove
the existence of severe hypoxia at birth. The remaining five
when present collectively suggest intrapartal timing but are
not specific to asphyxial insults. These efforts help to truly
identify intrapartum hypoxic events and other pathologies
responsible for CP. Recently, cord blood gases, placental
pathologies and neonatal brain imaging allow better
identification of antepartum etiologies. Additionally,
definition of acute hypoxia and its correlation with neonatal
nucleated red blood cells increase in chronic hypoxic
events can be used to differentiate between acute and
chronic pathologies
7-8
.
Relationship between neonatal encephalopathy and
cerebral palsys
Neonatal encephalopathy and HIE are related to CP and long
term neurologic deficits specifically in term and near term
infants in whom neurologic signs can be accurately
recognized, classified, and scientifically studied


****t is a non progressive neuromuscular disorder causing mild to severe disabilities throughout life.This condition is
manifested as a group of persisting qualitative motor disorders which appear in young children due to damage to the
brain during delivery or due to some pathological conditions in the intrauterine life.The neuroligical problems are
multiple but non progressive in nature.Approximately 2 per 100 live birth is having this problem.This disease is having no
hereditary tendency.

Causes of cerebral palsy:

1) Injury to the brain during delivery.

2) As a complication of forceps delivery.

3) Lack of oxygen supply to the baby during delivery.

4) Infections during delivery.

Signs and symptoms of cerebral palsy:--

The signs and symptoms may not be similar in all babies affected.Depending upon the damage to the brain there may be
mild to severe lesions.

Mild cases:- 20% children will have mild disability.

Moderate cases:-50% cases are having moderate disability.The affected children require self help for assisting their
impaired ambulation capacity.

Severe cases:-About 30% of the affected children are totally incapacited and bedridden and they allways need care from
others.

Abnormal findings in cerebral palsy:-

1,Abnormal neonatal reflexes.

2,Stiffness of all muscles with awkward motion.

3,Extention of extremities on vertical suspension of the infant.

4,Scissoring of the lower limbs due to spasm of the adductor muscles of the thigh.

5,In severe cases the back bend backwards like and arch.

6,May have total or partial paralysis.

7,Arrest of neurological and behavioral developement.

8,Swallowing may be difficult in some cases.

9,Drooling of saliva.

10,Mild to severe mental retardations.

11,Abnormal movements are seen in some cases.

12,Tremors with typical movements.

13,If cerebellum is affected there will be loss of muscle tone with difficulty in walking.

14,Complete or partial loss of hearing.

15,Speech may be affected.

16,Squint and other visual problems may be associated.

17,Convulsions may be seen in some children.

Cerebral palsy is diagnosed by detailed clinical examination and by eliminating other similar diseases like brain tumour,
progressive atrophy ect.All investigations like CT scan,MRI and routine investigations are needed to ruleout other
diseases.

Management of carebral palsy:--

General management:

This includes proper nutrition and personal care. Symptomatic medicines are needed to reduce convulsions and muscle
stiffness. Diazepam can reduce spasticity and athetosis.

Dantrolene sodium helps to relax skeletal muscles.

Physiotherapy:

Here massage,exercise, hydrotherapy and ect are needed.Special training is given to train walking,swallowing and
talking.The affected children are also trained to hold articles for routine activities.

Rehabilitation:

Moral and social support should be given to these children.They should be send to special schools where special training
can be given by trained staff.Mentally retarded children need special training.Depending up on the disabitity special
instruments and machines are given for locomotion and to assist their daytoday activities.

Occupational therapy:

This is given by occupational therapists.They train the disabled people to do some suitable works so that these people
can have their own income.

****Cerebral Palsy
What is cerebral palsy?
Cerebral Palsy (CP) is caused by birth injuries that affect the central nervous system, also called static
encephalopathy. Less than 1% of children are born with this type of injury. Almost half the children affected
by cerebral palsy develop hypertonia (excessive muscle tension) or spasticity (excessive muscle tension with
increased tendon reflexes). This is usually caused by damage to the white matter of the brain. Other affected
children can have mixed cerebral palsy, experiencing multiple symptoms with a spastic component. Cerebral
palsy can result in irreversible damage and dysfunction of the nervous system.
Causes of cerebral palsy
Many cases of CP have unknown causes. The disorder occurs when there is abnormal development or damage
to areas in the brain that control motor function. It occurs in approximately three out of every 1,000 live births.
There are several types of injuries that can impair the nervous system, including:
Head injuries
Central nervous system infections
Episodes that obstruct the oxygen flow to the brain, such as near-drowning experiences
Cerebrovascular accidents, like stroke
Malnutrition
Heavy metal ingestion
Symptoms of cerebral palsy
The following are the most common symptoms of CP. However, each child may experience symptoms
differently. The child may have muscle weakness, poor motor control, or have shaking, also called spasticity, of
the arms or legs. Muscle stiffness in the form of stiff legs or clenched fists may also be seen. Cerebral palsy is
classified according to the kind of motor function the child may have, including the following:
There are three ways that spasticity, or excessive tightening of muscles, can present itself in children suffering
from cerebral palsy:
Spastic diplegia, where the lower limbs are more involved than the upper. This typically affects premature
children, born before 32 weeks gestation.
Spastic quadriplegia, where all four limbs are involved equally. This typically affects children born closer to term.
Spastic hemiplegia, where only one side of the body is involved. This typically affects children who have a
history of ventricular bleeding that reaches their brain tissue, causing injury.
Children with CP may have additional problems, including the following:
Seizures
Vision, hearing, or speech problems
Learning disabilities and behavior problems
Mental retardation
Respiratory problems
Bowel and bladder problems
Bone abnormalities, including scoliosis (a lateral, or sideways, curvature and rotation of the back bones, giving
the appearance that the person is leaning to one side)
Babies with cerebral palsy are often slow to reach developmental milestones, such as learning to roll over, sit,
crawl, or walk. They may also have certain reflexes present that normally disappear in early infancy. The
symptoms of CP may resemble other conditions. Always consult your child's physician for a diagnosis.
Treatment for cerebral palsy
Baclofen (Liorisol) Baclofen is a muscle relaxant. It can be absorbed into the bloodstream when taken
orally, or it can be inserted directly into the cerebrospinal fluid (CSF). This method was recently approved by
the FDA, and is particularly effective because it delivers the drug directly to the target site in the spinal cord.
To deliver baclofen to the CSF, an access device must be implanted underneath the skin and fat of the
abdominal wall, requiring a two inch incision above the waistline. After the device is implanted, a needle is
used to place a small, flexible tube into the lower backs spinal fluid column near the targeted muscles. A child
is usually required to stay in the hospital for a few days to recover from the procedure and allow physicians to
monitor their progress. The device itself is a small titanium disk, about one inch thick and three inches wide. It
contains a refillable reservoir for the drug and a computer chip that regulates the dose. An alarm sounds when
the device needs to be refilled, the battery is low or the pump is not delivering the drug. The pump should be
refilled and medication adjusted every two to three months.
Therapeutic electrical stimulation (TES) TES is a type of electrical stimulation used at night while
patients are sleeping. It increased blood flow to weakened muscles to allow the body to deliver more growth
factors and nutrients to repair damaged tissue. This process usually takes between three and six months.
Children usually undergo physical therapy in conjunction with the treatment to increase muscle strength.
Selective Dorsal Rhizotomy (SDR) The SDR technique involves cutting some of the sensory nerve fibers
that come from the muscles and enter the spinal cord. A five to six inch incision is made along the center of the
lower back just above the waist in order to expose the nerves and locate the abnormal portions of nerve fiber
that need to be cut. This allows better balance in the spinal cord and reduces spasms, but does require a
commitment to physical therapy following treatment.